Markers and Mechanisms of Individual Differences in Cortico-Cardiac Covariation

对潜在威胁的认知处理几乎可以立即加速心脏活动。虽然已知皮质和心脏过程相互影响并相互影响（皮质-心脏共变），但我们不知道为什么皮质-心脏共变在某些个体中比在其他个体中更强。皮质-心脏共变的个体差异与焦虑的个体差异有关，因此对我们理解性格焦虑和焦虑障碍尤为重要。本文提出了两项健康参与者的研究，试图阐明皮质-心脏共变的标志物和机制。研究1的主要目的是检验先前报道的滞后单试验EEG和心率的受试者内相关性是否为皮质-心脏共变与焦虑相关提供了一个稳定有效的特征标记。N = 67名被试执行了几个范式（赌博任务、时间估计任务和恐惧条件反射范式），这些范式在脑电图上唤起了很好的特征特征，并评估了心率和脑电图-心率共变和性格焦虑的测量。6个月后执行相同的范例。根据收集到的数据，我们将采用多特征-多方法和交叉滞后面板方法，对不同测量方法（脑电图-心率共变、刺激诱发心率反应、心率变异性）评估的皮质-心脏共变的重测信度、收敛效度、构建效度和预测效度（即焦虑效度）进行评估。研究2的主要目的是研究皮质-心脏共变的潜在机制，并通过实验测试皮质-心脏共变的个体差异是否会导致焦虑的个体差异，反之亦然。在这项研究中，N = 148名参与者在电击威胁和控制条件下执行赌博任务。重要的是，我们打算通过双盲和安慰剂控制摄入艾司西酞普兰（10毫克），从药理学上改变皮质-心脏共变，这种物质可能通过调节血清素活性来影响皮质对心脏的影响。通过评估(A)（药理学诱导的）皮质-心脏共变的改变是否介导休克预期期间焦虑的主观体验，或(B)（休克威胁诱导的）焦虑的改变是否介导皮质-心脏共变的变化，可以推断焦虑和皮质-心脏共变之间的因果关系。综上所述，研究1和研究2提示，结合脑电图-心率测量评估的皮质-心脏共变是否反映了一种稳定的特征和经历焦虑的危险因素。这两项研究都将为大脑与心脏交流的一般机制以及皮质-心脏共变的个体变异机制提供重要的见解。

The mere cognitive processing of a potential threat may almost immediately accelerate cardiac activity. Although cortical and cardiac processes are known to affect each other and covary (cortico-cardiac covariation), we do not know why cortico-cardiac covariation is stronger in some individuals than in others. Individual differences in cortico-cardiac covariation relate to individual differences in anxiety and are thus particularly important for our understanding of dispositional anxiety and anxiety disorders. Here, two studies with healthy participants are proposed in an attempt to shed light on markers and mechanisms of cortico-cardiac covariation. The main goal of study 1 is to test whether previously reported within-subject correlations of time-lagged single-trial EEG and heart rate provide a stable and valid trait-marker for cortico-cardiac covariation with relevance for anxiety. N = 67 participants perform several paradigms (gambling task, time estimation task and fear conditioning paradigm) that evoke well-characterized signatures in EEG, heart rate and measures of EEG-heart rate covariation and dispositional anxiety is assessed. The same paradigms are performed 6 months later. With the collected data the re-test reliability, convergent, construct and predictive (i.e. anxiety) validity of cortico-cardiac covariation as assessed with various measures (EEG-heart rate covariation, stimulus-evoked heart rate responses, heart rate variability) and various paradigms will be assessed using multi-trait-multi-method and cross-lagged panel approaches. The main goal of study 2 is to investigate underlying mechanisms of cortico-cardiac covariation and to experimentally test whether individual differences in cortico-cardiac covariation contribute to individual differences in anxiety or vice versa. In that study, N = 148 participants perform a gambling task during threat-of-shock and control conditions. Importantly, we intend to pharmacologically alter cortico-cardiac covariation by double blind and placebo-controlled intake of escitalopram (10 mg), a substance that presumably affects cortical influences on the heart by modulating serotonin activity. By assessing whether (A) (pharmacologically induced) alterations of cortico-cardiac covariation mediate the subjective experience of anxiety during the anticipation of shocks or (B) whether (threat-of-shock induced) alterations of anxiety mediate changes in cortico-cardiac covariation, inferences about causal relationships between anxiety and cortico-cardiac covariation can be made. In combination, studies 1 and 2 thus inform, whether cortico-cardiac covariation as assessed with combined EEG-heart rate measurements reflects a stable trait and a risk factor for experiencing anxiety. Both studies will provide important insights into the general mechanisms by which the brain communicates with the heart and into the mechanisms of individual variation in cortico-cardiac covariation.